Retinoid embryopathy in the macaque exhibits many similarities to the malformation syndrome observed in humans following ingestion of retinoic acid during pregnancy. This syndrome involves defects of the craniofacial skeleton, particularly the external ears, as well as abnormalities of the cerebellum, heart, and thymus. All of these tissues receive cellular contributions from the cranial neural crest, a population of cells that appears in the primate embryo during a narrow developmental window (Stages 10-13, 8-31 somites). Studies were carried out in this model to study the effect of a known teratogenic dosing regimen of 13-cis retinoic acid on the ontogeny of the cranial neural crest cells and their early derivatives. Following treatment (5-10 mg/kg/day, gestational day [GD] 12-25), embryos were collected by hysterotomy on GD 25 to 29 (Stages 10-13). Histological sections were examined for general morphological features and status of the basement membrane (collagen-IV immunostaining). The immunoreactivity of neural cell adhesion molecule (N-CAM) in adjacent step-serial sections facilitated the identification of migratory neural crest cells and cranial pre-ganglia. Excessive cell death was noted in the neuroepithelium at GD 25, particularly in the hindbrain. GD 27 and 28 embryos exhibited an apparent reduction and/or delay in the emigration of cranial crest cells destined to populate the second, third, and fourth pharyngeal arches. At GD 29 the otic vesicle was still open to the ectoderm, small in size, and shifted rostrally and laterally. There was also significant shortening of the rhombomeres of the hindbrain and a reduction in the size of the pharyngeal arches. Together these results show that retinoic acid causes defects in the cynomolgus monkey by influencing the behavior of cranial neural crest cells and the normal developmental program of the hindbrain and the pharyngeal arches. *KEY* Pathogenesis, Cranial neural crest, Immunocytochemistry